Fetal Origins of Adult Disease

Calkins, Kara; Devaskar, Sherin U.

doi:10.1016/j.cppeds.2011.01.001

Cited by 651Birth, Development, and HealthPregnancy and preeclampsia studiesPrenatal Substance Exposure Effects

Fetal Origins of Adult Disease

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Calkins, Kara, Devaskar, Sherin U.·2011·Current Problems in Pediatric and Adolescent Health Care

DOI 10.1016/j.cppeds.2011.01.001PMC PMC4608552

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Abstract

Dr. David Barker first popularized the concept of fetal origins of adult disease (FOAD). Since its inception, FOAD has received considerable attention. The FOAD hypothesis holds that events during early development have a profound impact on one's risk for development of future adult disease. Low birth weight, a surrogate marker of poor fetal growth and nutrition, is linked to coronary artery disease, hypertension, obesity, and insulin resistance. Clues originally arose from large 20th century, European birth registries. Today, large, diverse human cohorts and various animal models have extensively replicated these original observations. This review focuses on the pathogenesis related to FOAD and examines Dr. David Barker's landmark studies, along with additional human and animal model data. Implications of the FOAD extend beyond the low birth weight population and include babies exposed to stress, both nutritional and nonnutritional, during different critical periods of development, which ultimately result in a disease state. By understanding FOAD, health care professionals and policy makers will make this issue a high health care priority and implement preventive measures and treatment for those at higher risk for chronic diseases.

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Some effects of early environmental exposure may be mediated by epigenetic mechanisms.
“Some of these effects may be mediated by epigenetic mechanisms.66,67”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [66]
Neonates exposed to HDP might have higher blood pressure in adolescence than neonates from healthy pregnancies.
“Neonates exposed to HDP might have higher blood pressure when entering adolescence than neonates from healthy pregnancies205–208.”
From A global view of hypertensive disorders and diabetes mellitus during pregnancy (2022) · cites this paper as [205]
The References section lists a study of blood pressure in 12-year-old children born after maternal preeclampsia, but gives no findings or comparison with children from healthy pregnancies. The Premature Infant section discusses higher offspring blood pressure after other prenatal exposures, not hypertensive disorders of pregnancy. Our copy therefore does not establish the claimed comparison. (LLM, conf=0.70)
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Impaired PI 3-kinase activation in adipocytes from early growth-restricted male rats
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Size at Birth, Fat-Free Mass and Resting Metabolic Rate in Adult Life
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In Utero Exposures and Breast Cancer: a Study of Opposite-Sexed Twins
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High Serum Leptin Concentrations during Catch-Up Growth of Children Born with Intrauterine Growth Retardation
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Expression of PDX-1 Is Reduced in Pancreatic Islets from Pups of Rat Dams Fed a Low Protein Diet during Gestation and Lactation
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Non‐human primate fetal kidney transcriptome analysis indicates mammalian target of rapamycin (mTOR) is a central nutrient‐responsive pathway
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Self-reported birth weight and subsequent risk of colorectal cancer.
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Polymorphism in the Growth Hormone Gene, Weight in Infancy, and Adult Bone Mass
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Perturbed skeletal muscle insulin signaling in the adult female intrauterine growth-restricted rat
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Birth size and colorectal cancer risk: a prospective population based study
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Depot-Specific Effects of Early Growth Retardation on Adipocyte Insulin Action
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No evidence for a major β-cell dysfunction in young adults born with intra-uterine growth retardation
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Early exercise regimen improves insulin sensitivity in the intrauterine growth-restricted adult female rat offspring
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Glucose transporter isoform-3-null heterozygous mutation causes sexually dimorphic adiposity with insulin resistance
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Size at birth and lipoprotein concentrations in adulthood: two prospective studies in Latin American cities
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A Study of Relationships Between Single Nucleotide Polymorphisms from the Growth Hormone-Insulin-like Growth Factor Axis and Bone Mass: the Hertfordshire Cohort Study
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‘Thinfat’ phenotype in newborns
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[18]Nyirenda MJ Lindsay RS Kenyon CJ Burchell A Seckl JR Glucocorticoid exposure in late gestation permanently programs rat hepatic phosphoenolpyruvate carboxykinase and glucocorticoid receptor expression and causes glucose intolerance in the adult offspring J Clin Invest 1988 101 2174 81 9593773 PMC508805

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Authors: Calkins, K., & Devaskar, S. U.
Affiliations: University of California, Los Angeles (US)
ORCID: Calkins, Kara
Devaskar, Sherin U.
Venue: Current Problems in Pediatric and Adolescent Health Care
Publisher: Elsevier BV
Published: 2011-07
Volume: 41
Issue: 6
Pages: 158-176
ISSN: 1538-3199 (ISSN-L)
1538-5442
DOI: 10.1016/j.cppeds.2011.01.001
PMC: PMC4608552
OpenAlex: W2070872186
Cited by: 651
References: 156
Citations by year: 2026: 20 · 2025: 39 · 2024: 52 · 2023: 43 · 2022: 70 · 2021: 57 · 2020: 65 · 2019: 55 · 2018: 41 · 2017: 29 · 2016: 46 · 2015: 35 · 2014: 29 · 2013: 33 · 2012: 21
FWCI: 4.24
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Current problems in pediatric and adolescent health care (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-33997, R01HD025024, HD25024, HD 41230, K12HD00140, R01HD041230, HD-046979, K12HD001400, R01HD033997, R01HD046979)
Topics: Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
Keywords: fetal origins of adult disease, Barker hypothesis, low birth weight, fetal growth restriction, coronary artery disease, hypertension, obesity, insulin resistance, developmental origins of health and disease, chronic disease risk, birth cohort studies, animal models
MeSH terms: Chronic Disease, Female, Humans, Infant, Low Birth Weight, Infant, Newborn, Male, Pregnancy, Prenatal Exposure Delayed Effects, Risk Factors, Genetic Predisposition to Disease, Fetal Development, Epigenomics

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